Is lactic acid what makes me sore two days after a hard session?
No: this opinion piece agrees blood lactic acid is gone within an hour and does not track soreness; its idea of a local lactate role in the muscle spindle is untested (C).
Sonkodi starts from the history: the build-up of lactic acid used to be blamed for muscle fatigue and delayed-onset muscle soreness (DOMS), studies in the 1980s largely refuted that role, and the belief is still widely held.
He restates the refutation in its own terms — concentric exercise has the higher metabolism yet causes no DOMS, eccentric exercise causes it; lactic acid returns to pre-exercise levels within an hour after exercise and its timeline does not match the soreness, after level or downhill running; lactic acid may contribute to acute soreness after intense exercise, not to the delayed kind.
He then argues that lactate still matters if a "neurocentric" view is taken.
The argument rests on his own earlier theory that DOMS is an "acute compression proprioceptive axonopathy": during unaccustomed or strenuous repetitive eccentric contractions under an acute stress response, the proprioceptive nerve terminals in the muscle spindle (type Ia, with Piezo2 ion channels) are micro-damaged — a painless primary phase inside the spindle — followed by a secondary, painful phase of damage and inflammation in the muscle outside it.
In this piece he proposes, by analogy with the astrocyte-neuron lactate shuttle in the brain, that intrafusal satellite cells feed the strained spindle neurons with lactate, that excessive acidosis and lactate then impair glutamate release at the Ia terminals and, through acid-sensing ion channels on type II fibres, add to impaired proprioception and increased pain, and that in the secondary phase lactate potentiates bradykinin, an essential player in the mechanical hyperalgesia of DOMS.
His conclusion: lactate "seems to have an essential role in the initiation" of DOMS within the spindle.
Our reading: this is the only current argument for a lactate role in soreness that the base has found, and it is a single author's chain of hypotheses on top of his own unproven theory; it is not evidence that lactate causes soreness, and it explicitly agrees that blood lactic acid does not.
For PHYS-06 and PHYS-23 it should be named as a live hypothesis, not as a dissent of weight.
Protocol
Key Results
What the author accepts (the classical refutation, as he summarises it):
| Point | As stated |
|---|---|
| History | lactic acid build-up was the accepted cause of DOMS until the early 1980s; studies in the 1980s largely refuted it |
| Contraction type | concentric exercise has higher metabolism and no DOMS; eccentric exercise causes DOMS |
| Time course | lactic acid returns to pre-exercise levels within an hour; the blood lactate timeline does not correlate with the soreness timeline, after level or downhill running |
| Remaining role | lactic acid may contribute to acute muscle soreness after intense exercise, due to fatigue (Léger et al.) |
| DOMS time course | pain evolves in about 8 h, peaks 1 or 2 days later and subsides in 7 days |
What the author proposes (hypotheses, untested in people):
| Phase | Proposal |
|---|---|
| Primary damage (inside the spindle, painless) | unaccustomed eccentric work under an acute stress response micro-damages type Ia proprioceptive terminals (Piezo2 channelopathy, impaired glutamate release); an astrocyte-neuron-like lactate shuttle from intrafusal satellite cells nourishes the strained neurons; excess acidosis and lactate impair glutamate release and, via ASIC3 channels on type II fibres, add to impaired proprioception and nociception; proposed to last 2-3 days without soreness if alone |
| Secondary damage (outside the spindle, painful) | extrafusal micro-damage with C-fibre pain; lactate potentiates bradykinin, which is essential for the mechanical hyperalgesia of DOMS |
| Why concentric work gives no DOMS | less intrafusal loading and lower intrafusal metabolism, not lower whole-muscle metabolism |
| Conclusion | lactate "seems to have an essential role in the initiation of the primary damage phase" of DOMS |
Mechanisms
Practical Application
Limitations
How this entry was checked and changed
expert opinion by the rubric: one author's argued hypothesis, resting mostly on his own earlier theory papers and on analogies from brain metabolism